Figure 1.

The effect of IL-17A deficiency on kidney injury and Th1/Th2 responses on day 6 of GN. Six days after receiving anti-GBM globulin, IL-17A^−/− mice had fewer abnormal glomeruli (A); decreased crescent formation (B); and attenuated glomerular accumulation of CD4⁺ T cells, macrophages, and neutrophils (C) compared with WT animals. D: Expression of P-selectin was down-regulated in glomeruli of IL-17A^−/− compared with WT animals with GN. ICAM-1 was expressed at low levels in glomeruli of normal mice without GN (0.5 ± 0.01 average score) but was not up-regulated in WT or IL-17A^−/− animals on day 6 of GN. IL-17A deficiency had no effect on the production of IFN-γ (E) by antigen-stimulated splenocytes, but it did increase the production of IL-4 (F). G and H: Representative photomicrographs of glomerular injury on day 6 of GN, showing hypercellularity, segmental proliferation/necrosis, and capillary wall/basement membrane thickening in WT animals (G) and less severe disease in IL-17A^−/− mice (H), as assessed on Bouin's-fixed paraffin-embedded periodic acid Schiff–stained kidney sections. I and J: Representative photomicrographs of glomerular P-selectin expression on day 6 of GN, showing moderate expression in WT mice (I) and decreased expression in IL-17A^−/− animals (J), as assessed by immunofluorescence on frozen kidney sections. Original magnification, ×400 (G–J). gcs, glomerular cross section. Mϕ, macrophages. *P < 0.05, **P < 0.01.